Pathology Flashcards
Increase in pressure in the heart lead to this:
Pressure-overload hypertrophy
Pressure overload hypertrophy is manifest by:
concentric increase in ventricular wall thickness
- new sarcomeres parallel to old ones (stacked like paper in a notebook)
Excess volume affects the heart by:
Volume overload hypertrophy
- ventricular dilation
How is volume-overload hypertrophy manifest?
ventricular dilation (wall may me more, less or same thickness) - new sarcomeres are positioned in series with existing sarcomeres
How does hypertrophy change normal cardiac function?
Requires more O2 and other metabolites (increased workload)
- hypertrophy does not supply additional coronary capillaries (less supply)
Hypertrophic/Dilated Heart characteristics:
- increase heart size/mass
- increase protein synthesis
- fibrosis
- inadequate vasculature
- –> leads to Cardiac dysfunction
Cardiac Dysfunction is characterized by:
- systolic or diastolic heart failure
- arrhythmias
- neurohumoral stimulation
dyspnea
shortness of breath
orthopnea
dyspnea when lying down
improved by standing
What is stable angina?
imbalance of cardiac perfusion (low) compared with cardiac demand (higher)
- during stress only: emotional excitement, exercise…
- relieved by rest
What drug can treat stable angina?
nitroglycerin
- strong vasodilator that increases perfusion
What is prinzmetal angina?
coronary artery spasm causes periodic myocardial ischemia
- unrelated to physical activity, HR, or BP
What drugs treat prinzmetal angina?
Vasodilators: nitroglycerin, Ca++ channel blockers
What is unstable angina?
Increasingly frequent pain of prolonged duration that occurs even at rest (unlike stable angina)
- usually due to disrupted atherosclerotic plaque with mural thrombosis (possibly embolism or vasospasm)
- preinfarction angina
What are the gross morphological changes due to MI at: - 4 hours - 24 hours - 1 week - 2 weeks - 1 month > 2months
4 hours: no gross features
24 hours: dark mottling (blood spots, bruise)
1 week: yellow-tan softening; hyperemic, red borders
2 weeks: red-gray depressed infarct borders
1 month: gray-white scar, outside moving to core
>2 months: scar complete, can no longer age
What are the histological features due to MI at: - 4 hours - 24 hours - 1 week - 2 weeks - 1 month > 2 months
4 hours: none, possible wavy fibers of early coagulation necrosis
24 hours: coagulation necrosis, myocyte hypereosinophilia, contraction band necrosis, early neutrophils
1 week: macrophage infiltrate, phagocytize dead cells
2 weeks: granulation tissue
1 month: increased collagen deposition
What happens to the heart in hypertrophic cardiomyopathy?
- thick walled, poorly compliant L ventricle
- septum thicker than outer wall (3:1)
- usually without dilation
- hypercontracting
- diastolic dysfunction (reduced filling –> low stroke volume)
Histologic features of HCM
Hypertrophic Cardiomyopathy
- myocyte hypertrophy
- haphazard disarray of contractile elements (myofiber disarray)
- fibrous replacement of myocytes in ventricular wall
Treatment for HCM
- Beta blockers: decrease contractility, HR
Clinical course/complications of HCM
variable
-most patients asymptomatic:
- atrial fibrillation, mural thrombus (embolization and stroke), cardiac failure, ventricular arrhythmias, sudden cardiac death
may have mitral valve prolapse/insufficiency due to high contractility an pressure of ventricle
Gene mutations in HCM are:
code for sarcomere proteins
- B-myosin heavy chain
- cardiac troponin-T
- myosin binding protein C
- alpha-topomyosin
What is DCM?
Dilated Cardiomyopathy
- progressive cardiac dilation
- systolic dysfunction (contraction)
What is HCM?
Hypertrophic Cardiomyopathy
- thickened ventricular wall due to myocyte hypertrophy
- diastolic dysfunction (trouble relaxing)
- decreased compliance/diastolic filling
What causes DCM?
- sometimes genetic
- myocarditis
- alcohol/chemo toxicity
- peri-partum
How does alcohol affect the heart?
Metabolism to acetaldehyde–> toxic to myocardium
Thiamine deficiency –> beriberi heart disease
Clinical course of DCM:
slowly progressive
- dyspnea, easy fatigability, poor exertional capacity
- markedly decreased ejection fraction
- mural thrombus formation –> poss.embolism
2*: mitral regurgitation, arrhythmia
What is amyloidosis?
deposition of abnormal substance in the heart
- eosinophilic deposits surround cardiac myocytes and capillaries
- shows apple green birefringence under polarized light with congo red stain
Causes of fibrinous pericarditis
acute MI postinfarction Dressler syndrome uremia chest radiation rheumatic fever SLE trauma
What is characteristic of fibrinous pericarditis?
loud pericardial friction rub
pain, systemic fever suggest CF present as well
Acute infective endocarditis differs from subacute IE in that:
Acute: normal heart valve and highly virulent pathogen
Subacute: abnormal heart valve and less virulent pathogen
Most common pathogen for subacute IE:
Streptococcus viridans
normal oral flora
Common pathogen for IE affecting already damaged heart valves:
Staph aureus
Pathogen responsible for IE in IV drug users:
S. aureus
HACEK bacteria are:
bacteria of the normal oral flora Haemophilus Actinobacillus Cardiobacterium Eikenella Kingella
Pathogen responsible for IE infection of prosthetic heart valves
Coagulase neg Staphylococcus
S. epidermidis
